Research in the Section on Neuroanatomy analyzes the function of the basal ganglia to understand how the striatum processes information from the cerebral cortex. The affects of this system on purposive behavior are determined by the relative activity of direct and indirect output neurons of the striatum, which have antagonistic effects on basal ganglia output pathways. We established that D1 and D2 dopamine receptor subtypes are segregated to neurons contributing to the direct and indirect output pathways, respectively. Ongoing research examines the regulation of these neurons with quantitative in situ hybridization, measuring alterations in gene expression in responses to pharmacologic manipulation of dopamine and other transmitter. We found that dopamine oppositely regulates the activity of the direct and indirect striatal output pathways, by elevating activity through D1 receptors and suppressing activity through D2 receptors. Combined activation of both receptors results in a potentiated activation of the direct striatal output pathway by intercellular interactions between D1- and D2- containing striatal neurons. These findings advance models of neurologic disease and mental disorders, including Parkinson's disease, attention deficit disorder, and schizophrenia. Additional insight into the regulation of striatal output neurons comes from the finding that the opiate peptide dynorphin, expressed in D1-containing striatal output neurons, inhibits the D1-mediated effects resulting from treatment with the indirect dopamine agonist cocaine. These interactions between striatal opiate and dopamine systems in response to cocaine are developed as animal models of drug abuse.